Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis

C E Richardson, J M Morgan, B Jasani, J T Green, J Rhodes, G T Williams, J Lindstrom, S Wonnacott, S Peel, G A O Thomas

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Abstract

Background: Ulcerative colitis (UC) is a disease largely of non-smokers, in which nicotine is of therapeutic value. The mode of action is unknown, but may involve nicotinic acetylcholine receptors (nAChRs) in the bowel wall. Aim: To investigate the presence of nAChRs in rectal mucosa, and the effect of smoking and nicotine on their expression. Design: Prospective case-control study.

Methods: In situ hybridization (ISH) and immunocytochemistry (ICC) were used to show alpha3 nAChRs in colonic mucosa. Rectal mucosa was examined from controls (n = 55) and patients with inactive UC (n = 62), both smokers and non-smokers, by ICC, using two antibodies to show the density and distribution of receptors in the mucosa. Non-smokers with UC (n = 43) were given transdermal nicotine or placebo patches for 6 months, and rectal biopsies, taken before and after treatment, were examined by ICC to show nAChRs.

Results: In normal colon, ISH and ICC showed alpha3 subunit in a wide variety of cells, including mucosal epithelium. In rectal biopsies, neither smoking nor nicotine influenced the expression of alpha3 immunoreactivity in epithelium, either in controls or UC. However, controls had a significantly greater density of immunodetectable mucosal epithelium alpha3 subunit, compared with UC patients.

Discussion: The presence of nAChRs in colonic epithelium may be pertinent to the beneficial effect of nicotine in UC, but since neither smoking nor nicotine treatment is associated with any change in the expression of epithelial alpha3 nAChRs, the effect may be due to functional changes in the receptor. The decreased number of alpha3 nAChRs in UC compared with controls may be related to an increased cell turnover in UC.

LanguageEnglish
Pages57-65
Number of pages9
JournalQJM: An International Journal of Medicine
Volume96
Issue number1
DOIs
StatusPublished - Jan 2003

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Nicotinic Receptors
Nicotine
Ulcerative Colitis
Smoking
Mucous Membrane
Epithelium
Immunohistochemistry
In Situ Hybridization
Biopsy
Case-Control Studies
Colon
Therapeutics
Placebos
Antibodies

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Richardson, C. E., Morgan, J. M., Jasani, B., Green, J. T., Rhodes, J., Williams, G. T., ... Thomas, G. A. O. (2003). Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. DOI: 10.1093/qjmed/hcg007

Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. / Richardson, C E; Morgan, J M; Jasani, B; Green, J T; Rhodes, J; Williams, G T; Lindstrom, J; Wonnacott, S; Peel, S; Thomas, G A O.

In: QJM: An International Journal of Medicine, Vol. 96, No. 1, 01.2003, p. 57-65.

Research output: Contribution to journalArticle

Richardson, CE, Morgan, JM, Jasani, B, Green, JT, Rhodes, J, Williams, GT, Lindstrom, J, Wonnacott, S, Peel, S & Thomas, GAO 2003, 'Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis' QJM: An International Journal of Medicine, vol. 96, no. 1, pp. 57-65. DOI: 10.1093/qjmed/hcg007
Richardson CE, Morgan JM, Jasani B, Green JT, Rhodes J, Williams GT et al. Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. QJM: An International Journal of Medicine. 2003 Jan;96(1):57-65. Available from, DOI: 10.1093/qjmed/hcg007
Richardson, C E ; Morgan, J M ; Jasani, B ; Green, J T ; Rhodes, J ; Williams, G T ; Lindstrom, J ; Wonnacott, S ; Peel, S ; Thomas, G A O. / Effect of smoking and transdermal nicotine on colonic nicotinic acetylcholine receptors in ulcerative colitis. In: QJM: An International Journal of Medicine. 2003 ; Vol. 96, No. 1. pp. 57-65
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abstract = "Background: Ulcerative colitis (UC) is a disease largely of non-smokers, in which nicotine is of therapeutic value. The mode of action is unknown, but may involve nicotinic acetylcholine receptors (nAChRs) in the bowel wall. Aim: To investigate the presence of nAChRs in rectal mucosa, and the effect of smoking and nicotine on their expression. Design: Prospective case-control study. Methods: In situ hybridization (ISH) and immunocytochemistry (ICC) were used to show alpha3 nAChRs in colonic mucosa. Rectal mucosa was examined from controls (n = 55) and patients with inactive UC (n = 62), both smokers and non-smokers, by ICC, using two antibodies to show the density and distribution of receptors in the mucosa. Non-smokers with UC (n = 43) were given transdermal nicotine or placebo patches for 6 months, and rectal biopsies, taken before and after treatment, were examined by ICC to show nAChRs. Results: In normal colon, ISH and ICC showed alpha3 subunit in a wide variety of cells, including mucosal epithelium. In rectal biopsies, neither smoking nor nicotine influenced the expression of alpha3 immunoreactivity in epithelium, either in controls or UC. However, controls had a significantly greater density of immunodetectable mucosal epithelium alpha3 subunit, compared with UC patients. Discussion: The presence of nAChRs in colonic epithelium may be pertinent to the beneficial effect of nicotine in UC, but since neither smoking nor nicotine treatment is associated with any change in the expression of epithelial alpha3 nAChRs, the effect may be due to functional changes in the receptor. The decreased number of alpha3 nAChRs in UC compared with controls may be related to an increased cell turnover in UC.",
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AU - Green,J T

AU - Rhodes,J

AU - Williams,G T

AU - Lindstrom,J

AU - Wonnacott,S

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N2 - Background: Ulcerative colitis (UC) is a disease largely of non-smokers, in which nicotine is of therapeutic value. The mode of action is unknown, but may involve nicotinic acetylcholine receptors (nAChRs) in the bowel wall. Aim: To investigate the presence of nAChRs in rectal mucosa, and the effect of smoking and nicotine on their expression. Design: Prospective case-control study. Methods: In situ hybridization (ISH) and immunocytochemistry (ICC) were used to show alpha3 nAChRs in colonic mucosa. Rectal mucosa was examined from controls (n = 55) and patients with inactive UC (n = 62), both smokers and non-smokers, by ICC, using two antibodies to show the density and distribution of receptors in the mucosa. Non-smokers with UC (n = 43) were given transdermal nicotine or placebo patches for 6 months, and rectal biopsies, taken before and after treatment, were examined by ICC to show nAChRs. Results: In normal colon, ISH and ICC showed alpha3 subunit in a wide variety of cells, including mucosal epithelium. In rectal biopsies, neither smoking nor nicotine influenced the expression of alpha3 immunoreactivity in epithelium, either in controls or UC. However, controls had a significantly greater density of immunodetectable mucosal epithelium alpha3 subunit, compared with UC patients. Discussion: The presence of nAChRs in colonic epithelium may be pertinent to the beneficial effect of nicotine in UC, but since neither smoking nor nicotine treatment is associated with any change in the expression of epithelial alpha3 nAChRs, the effect may be due to functional changes in the receptor. The decreased number of alpha3 nAChRs in UC compared with controls may be related to an increased cell turnover in UC.

AB - Background: Ulcerative colitis (UC) is a disease largely of non-smokers, in which nicotine is of therapeutic value. The mode of action is unknown, but may involve nicotinic acetylcholine receptors (nAChRs) in the bowel wall. Aim: To investigate the presence of nAChRs in rectal mucosa, and the effect of smoking and nicotine on their expression. Design: Prospective case-control study. Methods: In situ hybridization (ISH) and immunocytochemistry (ICC) were used to show alpha3 nAChRs in colonic mucosa. Rectal mucosa was examined from controls (n = 55) and patients with inactive UC (n = 62), both smokers and non-smokers, by ICC, using two antibodies to show the density and distribution of receptors in the mucosa. Non-smokers with UC (n = 43) were given transdermal nicotine or placebo patches for 6 months, and rectal biopsies, taken before and after treatment, were examined by ICC to show nAChRs. Results: In normal colon, ISH and ICC showed alpha3 subunit in a wide variety of cells, including mucosal epithelium. In rectal biopsies, neither smoking nor nicotine influenced the expression of alpha3 immunoreactivity in epithelium, either in controls or UC. However, controls had a significantly greater density of immunodetectable mucosal epithelium alpha3 subunit, compared with UC patients. Discussion: The presence of nAChRs in colonic epithelium may be pertinent to the beneficial effect of nicotine in UC, but since neither smoking nor nicotine treatment is associated with any change in the expression of epithelial alpha3 nAChRs, the effect may be due to functional changes in the receptor. The decreased number of alpha3 nAChRs in UC compared with controls may be related to an increased cell turnover in UC.

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